Pulmonary hypertension (PHT) is a condition that is characterized by thickened arterial walls of the vessels in the lung. The condition may be congenital, primary PHT where the initial lesion is in the lungs or acquired PHT from failure of other members of the cardiac-pulmonary axis. Congenital PHT is generally due to a left-right shunt associated with ventricular or atrial septal defects or patent ductus arteriosus. Primary PHT may be caused by emphysema, chronic asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, pulmonary embolism with parenchymal infarct and reactive pulmonary blood vessels or tissues. Some of the triggers for acquired PHT are exposure to toxins, infections, air pollutants, tobacco smoke, and residence at high altitudes. Whatever the nature, congenital, primary or acquired, PHT eventually leads to right ventricular hypertrophy with or without heart failure. Patients are able to compensate with conventional medical therapies and can stabilize for an indefinite time. Other patients afflicted with this condition die due to progressive heart decompensation or may require a heart/lung transplant.
While the underlying etiology of acquired PHT may not yet be known, one common factor leading to the condition may be that the pulmonary blood vessels and lung tissue are very sensitive to certain factors that trigger the development of the disease. Among these suspected factors are a preexisting condition of Raynaud's syndrome, appetite suppressants, cocaine, and congestive heart failure. Certain disease states such as emphysema, reactive airway disease, chronic obstructive pulmonary disease, HIV infection, scleroderma and systemic lupus erythematosus are often accompanied by PHT.
Treatment commonly is merely symptomatic. Methods of lowering of the vasculature's blood pressure in those patients with hypertension may give some relief.
U.S. Pat. No. 6,218,366 discloses a therapeutic method comprising administering ribose to a mammal in an effective amount to increase the tolerance of the mammal to hypoxia, wherein the hypoxia is due to cardiovascular disease, myocardial stunning, anaesthesia, surgical procedures, peripheral vascular disease, intermittent claudication, pulmonary dysfunction, physical exertion, pharmaceutical treatment, tachycardia or poisoning.
U.S. Pat. No. 6,420,342 discloses a nutritional composition, comprising ribose and folate in amounts which are effective to support total nucleotide metabolism, and 0.1 to eight grams of orotate per five grams of ribose.
WO/2006/050585 discloses a food product comprising at least one betine and L-arginine in a combined amount effective to induce and/or sustain a physiological increase in nitric oxide production in a mammal after ingesting said food product. This is claimed to be beneficial for the treatment of pulmonary hypertension by lowering the blood pressure.
The disadvantage of the known treatments is that there does not exist an optimal nutritional treatment that is focused on the problems related to pulmonary hypertension. Thus need remains for a nutritional therapy to limit the progression of pulmonary hypertension, whether congenital, primary or acquired.